Frank C. Greiss

Dynamics of Ventricular Ejection

Left ventricular ejection in open-chest, anesthetized dogs begins with an abrupt acceleration of blood into the ascending aorta, reaching an average maximum of 4,650 cm./sec./sec. Velocity reaches a sharp peak of 88 cm./sec. (average) within the first one-third to one-half of the ejection period. Deceleration is more gradual and continues to the closure of the aortic valve. The general pattern of the time-course recording is that of a triangle with its peak skewed into early systole and separated from a flat diastolic period of zero flow by a deep notch of backflow attending closure of the aortic valve. Ventricular pressure exceeds aortic pressure only during the brief period between the opening of the valve and peak systolic velocity, a period of approximately 45 per cent of the ejection period. This “positive” (headward) gradient represents the acceleration transient and explains the sharp rise in flow to a maximum in early systole. During the deceleration (terminal) phase of ventricular ejection, the pressure gradient is against the direction of flow. This reversal in pressure gradient brings about a gradual deceleration of flow to zero. These findings are considered experimental proof that the major phenomenon relating pressure and flow in the ascending aorta is that governing mass acceleration.

An Evaluation of Vasopressor Therapy for Maternal Hypotension during Spinal Anesthesia

During hypotension resulting from conduction anesthesia in gravid ewes, uterine blood flow (UBF) decreased roughly in proportion to the decrease in maternal blood pressure. Ephedrine or mephentermine significantly increased UBF over that accomplished by metaraminol. Presumably, the preferential effects of these agents were the result of increased cardiac output owing to inotropic and chronotropic actions. However, UBF never exceeded 90 per cent of prespinal levels with any vasoactive agent and, for a given maternal system, the UBF response was variable, generally increasing but frequently remaining constant or decreasing. For these reasons, all other methods of combating hypotension should be used initially. If vasopressors are still required, agents of choice are those whose principal mode of action lies in cardiac stimulation rather than peripheral vasoconstriction.

Uterine vascular changes during the ovarian cycle

Abstract Uterine blood flow (UBF) was monitored daily during 15 estrous cycles in 10 conscious ewes and flow patterns were correlated with other parameters of estrus, including ram receptivity. UBF increased eight- to twentyfold at estrus. A constant pattern of periestrus changes consisted of a series of isolated UBF spikes of short duration followed by an abrupt persistent increase preceding and extending into the period of ram receptivity. Thereafter, an abrupt decrease in UBF occurred during the estrus period followed by a more gradual decline during the remainder of the estrous cycle. These changes are apparently a result of the direct effects of estrogen and/or progesterone on the uterine vascular bed. Such effects are discussed in the light of available literature.

Uterine blood flow during early ovine pregnancy.

Abstract Left uterine artery blood flow was monitored from conception through 61 days of gestation in 11 ewes. From the conceptual estrus peak, uterine blood flow (UBF) decreased rapidly similar to the pattern during normal estrous cycle. A sharp progressive rise in UBF occurred on day 17 or 18 when the embryo was in the uterine cornu ipsilateral to the monitored artery. The rise was delayed when the embryo occupied the contralateral cornu. The significance of these observations is discussed in the light of autopsy findings and reported ovine embryologic development.

The effect of placental location on uterine artery flow velocity waveforms

We examined the effect of placental location with regard to flow velocity waveforms in the uterine arteries in 84 control and 28 hypertensive women during the third trimester of pregnancy. The ratio of systolic peak to end-diastolic frequency was obtained with a continuous-wave Doppler device and the placental location was determined by real-time ultrasonography. In both normal and hypertensive pregnancies with unilateral placental location the systolic/diastolic ratio of the ipsilateral uterine artery was significantly lower than the contralateral artery ratio [1.73 +/- 0.35 (systolic/diastolic ratio) versus 2.46 +/- 0.73, p less than 0.001, and 2.38 +/- 1.01 versus 4.04 +/- 1.77, p = 0.0012, respectively]. The physiologic and clinical significance of this finding is discussed.

Differential reactivity of the myoendometrial and placental vasculatures: Adrenergic responses☆

Abstract Adrenergic reactivity of the uterine vascular bed was compared in term pregnant ewes and castrated ewes receiving estradiol alone or in combination with progesterone. The myoendometrial vasculature (castrated uterus) was acutely sensitive to alpha-adrenergic stimulation and resistant to alpha-receptor blockade, demonstrated epinephrine reversal, and responded to beta-adrenergic stimulation with vasodilatation. The latter two responses were obliterated by propanolol, thus confirming the presence of beta-adrenergic receptors. None of the responses was changed by the hormonal background. The dominantly placental vasculature (term pregnant uterus) was less sensitive to alpha stimulation and was more sensitive to alpha blockade. Beta-adrenergic responses could not be demonstrated. In one pregnant ewe, the placental cotyledons were confined to one uterine horn. The responses of the non-placenta-containing horn (gravid myoendometrium) were most similar to those of the castrated uterus. These results indicate a basic difference in the vascular reactivity of the myoendometrium and the placenta and suggest that myoendometrial responses are similar in the pregnant and nonpregnant states.

Effects of Nitroglycerin and Nitroprusside on the Uterine Vasculature of Gravid Ewes

The effects of nitroglycerin (TNG) and sodium nitroprusside (SNP) on mean aortic pressure (MAP), uterine blood flow (UBF), uterine vascular conductance (UVC), and pulse rate (PR) were compared when the two agents were infused to prevent and treat hypertension induced by norepinephrine (NE) in gravid ewes. When infused alone, TNG, 19 üg/kg/min, decreased MAP 19 per cent and increased PR 33 per cent from control values (P lt; 0.05), but did not significantly change UBF or UVC. In comparison, SNP, 3 üg/kg/min, decreased MAP 20 per cent and increased PR 43 per cent (P lt; 0.05), and did not significantly change UBF or UVC. When given alone, four successive 2-min infusions of NE produced dose-related increase in MAP and decreases in UBF, UVC, and PR; values were significantly different from control with the two higher doses of NE. Although MAP, UBF, and UVC were still significantly changed from control levels when NE was given in the presence of the above infusions of TNG or SNP, MAP was lower and UBF and UVC were higher compared with when NE was given alone (P lt; 0.05). When given to control hypertension induced by a continuous infusion of NE, TNG or SNP produced uterine vasodilatation and significantly increased UBF. Nitroglycerin and SNP were equally effective in counteracting the maternal hypertension and antagonizing the uterine vascular effect of NE. It is concluded that TNG and SNP counteract uterine vasoconstriction resulting from alpha-adrenergic stimulation and do not produce a shunt of blood flow away from the uterine vasculature when used to control hypertension in gravid ewes.

The effect of prostaglandins and other vasoactive substances on uterine blood flow and myometrial activity.

The effects of prostaglandins (PGs), bradykinin, and adenosine on uterine blood flow (UBF) and intrauterine pressure (IUP) were investigated in conscious oophorectomized ewes. PGE1 and adenosine increased UBF to levels comparable to those induced by estradiol-17beta, whereas PGE2 and PGA1 achieved only 20 and 36 per cent of peak estradiol-induced levels, respectively. PGE1, PGE2, and adenosine all caused transient increases in IUP while PGA1 had no effect on myometrial activity. Bradykinin increased UBF to 60 per cent of peak estradiol-induced levels, with concomitant increases in IUP tonus. PGE2 and PGF2alpha decreased peak estrogen-induced UBF by 50 and 70 per cent, respectively, while inducing related increases in IUP. When compared with oxytocin, the effects of PGE2 at high flow appeared to be mediated only my myometrial activity, whereas PGF2alpha apparently caused vasoconstriction as well. These findings support the concept that PGE1 could play a role in mediating estrogen-induced uterine vasodilatation.

Stage IA squamous cell carcinoma of the uterine cervix

Abstract The microscopic pathology and clinical courses of 44 patients treated with radical hysterectomy and pelvic lymphadenectomy for equivocal or early invasive squamous cell carcinoma of the cervix were reviewed according to the classification of Frick and his associates. The incidence of major therapy complications was 14 per cent and all patients survived 5 or more years after therapy. Review of the literature on Stage IA lesions showed a 1.9 per cent incidence of lymph node metastases (103 patients), a 0.4 per cent recurrence rate in 243 patients treated conservatively, and a 1.0 per cent incidence of recurrence or evidence of primary spread beyond the cervix in 621 patients receiving all forms of therapy. From reported results, it would appear that equivocally invasive lesions and those lesions invasive up to 3 mm. without involvement of cervical lymphatics can be managed safely with conservative therapy.

Differential reactivity of the gravid uterine vasculatures: Effects of norepinephrine☆☆☆

Norepinephrine dose-conductance-response relationships were determined for the placental and nonplacental vasculatures of ewes between 95 and 130 days of gestation with the use of radioactive-labeled microspheres injected under flow meter guidance. The regression line for the placental circulation differed significantly from that for the nonplacental circulation (P less than 0.01). The decrease in nonplacental conductance was 30 to 45% of control greater than the decrease in placental conductance. These responses are consistent with the hypothesis that the site of placental vascular resistance is in vessels of larger caliber than those which are usually the primary site of resistance to blood flow.